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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">nefr</journal-id><journal-title-group><journal-title xml:lang="ru">Нефрология</journal-title><trans-title-group xml:lang="en"><trans-title>Nephrology (Saint-Petersburg)</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1561-6274</issn><issn pub-type="epub">2541-9439</issn><publisher><publisher-name>Pavlov First Saint-Petersburg State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.24884/1561-6274-2008-12-2-56-60</article-id><article-id custom-type="elpub" pub-id-type="custom">nefr-1061</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ СТАТЬИ. КЛИНИЧЕСКИЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES. CLINICAL INVESTIGATIONS</subject></subj-group></article-categories><title-group><article-title>КОНЦЕНТРАЦИЯ  АЛЬДОСТЕРОНА,  СОСТОЯНИЕ  ГЕМОСТАЗА  И  ЭНДОТЕЛИАЛЬНОЙ  ФУНКЦИИ  У  БОЛЬНЫХ  НА  ПРОГРАММНОМ  ГЕМОДИАЛИЗЕ  И  ВЛИЯНИЕ  НА  НИХ ТЕРАПИИ  СПИРОНОЛАКТОНОМ</article-title><trans-title-group xml:lang="en"><trans-title>CONCENTRATION  OF ALDOSTERONE,  STATE OF  HEMOSTASIS ANВ  ENDOTHELIAL FUNCTION  IN  PATIENTS ON  PROGRAMMED HEMODIALYSIS  AND  EFFECTS OF  EXPOSURE TO THERAPY WITH  SPIRONOLACTONE</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Карабаева</surname><given-names>А. Ж.</given-names></name><name name-style="western" xml:lang="en"><surname>Karabaeva</surname><given-names>A. Zh.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кафедра нефрологии и диализа факультета последипломного обучения </p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Есаян</surname><given-names>А. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Essaian</surname><given-names>A. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кафедра нефрологии и диализа факультета последипломного обучения </p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каюков</surname><given-names>И. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Kayukov</surname><given-names>I. G.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кафедра нефрологии и диализа факультета последипломного обучения </p><p>197022, Санкт-Петербург, тел.: (812)- 346-39-26, факс: (812)-234-91-91</p></bio><email xlink:type="simple">kaukov@nephrolog.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Санкт-Петербургский государственный медицинский уни­верситет им. акад. И.П. Павлова,  Санкт-Петербург</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2008</year></pub-date><pub-date pub-type="epub"><day>10</day><month>02</month><year>2008</year></pub-date><volume>12</volume><issue>2</issue><fpage>56</fpage><lpage>60</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Карабаева А.Ж., Есаян А.М., Каюков И.Г., 2008</copyright-statement><copyright-year>2008</copyright-year><copyright-holder xml:lang="ru">Карабаева А.Ж., Есаян А.М., Каюков И.Г.</copyright-holder><copyright-holder xml:lang="en">Karabaeva A.Z., Essaian A.M., Kayukov I.G.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://journal.nephrolog.ru/jour/article/view/1061">https://journal.nephrolog.ru/jour/article/view/1061</self-uri><abstract><p>ЦЕЛЬ ИССЛЕДОВАНИЯ. Изучить уровень концентрации альдостерона плазмы,состояние системы гемостаза и функции эндотелия у больных с хронической болезнью почек (ХБП) V стадии на программном гемодиализе и оценить влияние на них терапии спиронолактоном. ПАЦИЕНТЫ И МЕТОДЫ. 83 пациента с ХБП V стадии на программном гемодиализе. У обследованных определяли концентрацию альдостерона плазмы (КАП), оценивали функциональное состояние эндотелия с помощью биохимических маркеров – ингибитора активатора плазминогена 1 типа (PAI-1), тканевого активатора плазминогена (t-PA), эндотелина-1, состояние тромбоцитарного и коагуляционного звеньев гемостаза оценивали по морфофункциональной активации и агрегации тромбоцитов, концентрации фибриногена по Клауcсу, активности антитромбина-III (АТ-III), уровня D-димера методом латексной агглютинации до и после 6-месячного курса терапии спиронолактоном. РЕЗУЛЬТАТЫ. У всех больных исходно имелось значительное повышение уровня альдостерона крови – 478±99,96 пг/мл (норма - до 160,0±29,23 пг/ мл). На фоне терапии спиронолактоном отмечено достоверное снижение уровня альдостерона до 346,45±58,1 пг/мл (р=0,009), достоверное снижение активности маркеров эндотелиальной дисфункции: эндотелина-1 с 0,63±0,09 fmol/ml до 0,23±0,03 (р=0,002), PAI-1 с 5,69±0,24 до 3,06±0,25 U/ml (р&lt;0,001); повышение уровня t-PA с 5,03±0,3 до 5,64±0,3. Исследование системы гемостаза выявило активацию тромбоцитарного звена: повышение суммы активных форм тромбоцитов и увеличение числа тромбоцитов, вовлеченных в агрегаты, за счет образования внутрисосудистых агрегатов малого размера (р&lt;0,05), повышение концентрации фибриногена (р&lt;0,05) по сравнению с группой здоровых лиц, значения АТ-III находились на нижней границе референтных величин, 30% больных имели повышенный уровень D-димера. Достоверных изменений в показателях гемостаза после лечения спиронолактоном не выявлено. ЗАКЛЮЧЕНИЕ. Терапия спиронолактоном у больных на программном гемодиализе приводит к улучшению состояния эндотелиальной функции. При этом сохраняется дисбаланс в системе гемостаза, характеризующийся активацией тромбоцитов, напряжением в системе АТ-III, повышением уровня D-димера, что может повышать риск развития сосудистых катастроф у больных с хронической болезнью почек.</p></abstract><trans-abstract xml:lang="en"><p>THE AIM of the investigation was to study the level of the concentration of plasma aldosterone, the state of the hemostasis system and function of endothelium in patients with the V stage chronic kidney disease (CKD) on programmed hemodialysis and to estimate the effects of spironolactone therapy on them. PATIENTS AND METHODS. In the investigated 83 patients with V stage CKD on programmed hemodialysis the following indicators were studied: determination of the concentration of plasma aldosterone (CPA), assessment of the functional state of the endothelium using biochemical markers – plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (t-PA), endothelin-1, state of thrombocytic and coagulation link of hemostasis were estimated by morphofunctional activation and aggregation of thrombocytes, concentration of fibrinogen after Clauss, activity of antithrombin-III (AT-III), D-dimer level by the method of latex agglutinationb before and after 6-month course of therapy with spironolactone. RESULTS. All the patients initially had considerably elevated level of blood aldosterone -478±99.96 pg/ml (normal – up to 160.0±29.23 PG/MK0 pg/ml). Against the backgroung of spironolactone therapy there was a reliably decreased level of aldosterone up to 346.45±58.1 pg/ml (p=0.009), reliably decreased activity of the endothelial dysfunction markers: endothelin-1 from 0.63±0.09 fmol/ml to 0.23±0.03 (p=0.002), PAI-1 from 5.69± 0.24 up to 3.06± 0.25 U/ml (p&lt;0.001); elevation of the level of t-PA from 5.03±0.3 up to 5.64± 0.3. The investigation of the hemostasis system revealed activation of the thrombocytic link: increased sum of active forms of thrombocytes and greater number of thrombocytes involved in aggregates at the expense of the formation of intravascular aggregates of small size (p&lt;0.05), increased concentration of fibrinogen (p&lt;0.05) as compared with the group of healthy subjects, the value of AT-III was at the low border of the reference values, 30% of patients had higher level of D-dimer. No reliable changes in the indices of hemostasis after treatment with spironolactone were found. CONCLUSION. Spironolactone therapy in patients on programmed hemodialysis results in the better state of the endothelium function. The disbalance in the system of hemostasis remains the same, and is characterized by activation of thrombocytes, tension in the system AT-III, elevation of the D-dimer level, that might increase risk of the development of vascular catastrophies in patients with chronic kidney disease.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>хроническая  болезнь  почек</kwd><kwd>хронический  гемодиализ</kwd><kwd>альдостерон</kwd><kwd>фибринолитическая  система</kwd><kwd>система гемостаза</kwd><kwd>эндотелиальная дисфункция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>chronic kidney disease</kwd><kwd>chronic hemodialysis</kwd><kwd>aldosterone</kwd><kwd>fibrinolitic system</kwd><kwd>hemostasis system</kwd><kwd>endothelial dysfunction</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Collins AJ, Schuling L, Ma JZ, Herzog CH. Cardiovascular disease in end-stage renal disease patients. Am J Kidney Dis 2001; 38: S26–S29</mixed-citation><mixed-citation xml:lang="en">Collins AJ, Schuling L, Ma JZ, Herzog CH. Cardiovascular disease in end-stage renal disease patients. Am J Kidney Dis 2001; 38: S26–S29</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Schillaci G, Reboldi G, Verdechia P. High-normal serum creatinine concentration is a predictor of cardiovascular risk in essential hypertension. Arch Intern Med 2001; 161: 886–891</mixed-citation><mixed-citation xml:lang="en">Schillaci G, Reboldi G, Verdechia P. High-normal serum creatinine concentration is a predictor of cardiovascular risk in essential hypertension. Arch Intern Med 2001; 161: 886–891</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Garg AX, Clark FC, Haynes RB, House AA. Moderate renal insufficiency and the risk of cardiovascular mortality: results from the NHANES I. Kidney Int 2002; 61: 1486–1494</mixed-citation><mixed-citation xml:lang="en">Garg AX, Clark FC, Haynes RB, House AA. Moderate renal insufficiency and the risk of cardiovascular mortality: results from the NHANES I. Kidney Int 2002; 61: 1486–1494</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Weyer C, Yudkin JS, Stehouwer CD et al. Humoral markers of inflammation and endothelial dysfunction in relation to adiposity and in vivo insulin action in Pima Indians. Atherosclerosis 2002; 161: 233–242</mixed-citation><mixed-citation xml:lang="en">Weyer C, Yudkin JS, Stehouwer CD et al. Humoral markers of inflammation and endothelial dysfunction in relation to adiposity and in vivo insulin action in Pima Indians. Atherosclerosis 2002; 161: 233–242</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Festa A, D’Agostino R Jr, Tracy RP, Haffner SM. Elevated levels of acute-phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Diabetes 2002; 51: 1131–1137</mixed-citation><mixed-citation xml:lang="en">Festa A, D’Agostino R Jr, Tracy RP, Haffner SM. Elevated levels of acute-phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Diabetes 2002; 51: 1131–1137</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Meigs JB, Hu FB, Rifai N, Manson JE. Biomarkers of endothelial dysfunction and risk of type 2 diabetes mellitus. JAMA 2004; 291: 1978–1986</mixed-citation><mixed-citation xml:lang="en">Meigs JB, Hu FB, Rifai N, Manson JE. Biomarkers of endothelial dysfunction and risk of type 2 diabetes mellitus. JAMA 2004; 291: 1978–1986</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Rossi R, Cioni E, Nuzzo A et al. Endothelial-dependent vasodilation and incidence of type 2 diabetes in a population of healthy postmenopausal women. Diabetes Care 2005; 28: 702–707</mixed-citation><mixed-citation xml:lang="en">Rossi R, Cioni E, Nuzzo A et al. Endothelial-dependent vasodilation and incidence of type 2 diabetes in a population of healthy postmenopausal women. Diabetes Care 2005; 28: 702–707</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Widlansky ME, Gokce N, Keaney JF Jr, Vita JA. The clinical implications of endothelial dysfunction. J Am Coll Cardiol 2003; 42: 1149–1160</mixed-citation><mixed-citation xml:lang="en">Widlansky ME, Gokce N, Keaney JF Jr, Vita JA. The clinical implications of endothelial dysfunction. J Am Coll Cardiol 2003; 42: 1149–1160</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Epstein M. Аldosterone as a mediator of progressive renal dysfunction: evolving perspectives. Intern Med 2001 Jul; 40(7): 573–583</mixed-citation><mixed-citation xml:lang="en">Epstein M. Аldosterone as a mediator of progressive renal dysfunction: evolving perspectives. Intern Med 2001 Jul; 40(7): 573–583</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Epstein M. Aldosterone receptor blockade and the role of eplerenone: evolving perspectives. Nephrol Dial Transpl 2003; 18(10): 1984–1992</mixed-citation><mixed-citation xml:lang="en">Epstein M. Aldosterone receptor blockade and the role of eplerenone: evolving perspectives. Nephrol Dial Transpl 2003; 18(10): 1984–1992</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Weber KT. Aldosterone in congestive hear failure. N Engl J Med 2001; 345: 1689–1697</mixed-citation><mixed-citation xml:lang="en">Weber KT. Aldosterone in congestive hear failure. N Engl J Med 2001; 345: 1689–1697</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Fuller PJ, Young MJ. Mechanisms of mineralocorticoid action. Hypertension 2005; 46: 1227–1246</mixed-citation><mixed-citation xml:lang="en">Fuller PJ, Young MJ. Mechanisms of mineralocorticoid action. Hypertension 2005; 46: 1227–1246</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341: 709–717</mixed-citation><mixed-citation xml:lang="en">Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341: 709–717</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Gross E, Rothstein M, Dombek S, Juknis HI. Effect of Spironolactone on Blood Pressure and the Renin-Angiotensin-Aldosterone System in Oligo-Anuric Hemodialysis Patients. Am J Kidney Dis2005; 46(1): 94–101</mixed-citation><mixed-citation xml:lang="en">Gross E, Rothstein M, Dombek S, Juknis HI. Effect of Spironolactone on Blood Pressure and the Renin-Angiotensin-Aldosterone System in Oligo-Anuric Hemodialysis Patients. Am J Kidney Dis2005; 46(1): 94–101</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Saudan P, Mach F, Perneger Th et al. Safety of low-dose spironolactone administration in chronic haemodialysis patients. Nephrol Dial Transplant 2003; 18: 2359–2363</mixed-citation><mixed-citation xml:lang="en">Saudan P, Mach F, Perneger Th et al. Safety of low-dose spironolactone administration in chronic haemodialysis patients. Nephrol Dial Transplant 2003; 18: 2359–2363</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Arima S, Kohagura K, Xu HL et al. Nongenomic vascular action of aldosterone in glomerular microcirculation J Am Soc Nephrol 2003; 14 (9): 2253–2255</mixed-citation><mixed-citation xml:lang="en">Arima S, Kohagura K, Xu HL et al. Nongenomic vascular action of aldosterone in glomerular microcirculation J Am Soc Nephrol 2003; 14 (9): 2253–2255</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Norris K, Vaughn C. The role of rennin-angiotensin-aldosterone system in chronic kidney disease. Expert Rev Cardiovasc Ther 2003; 1 (1): 51–63</mixed-citation><mixed-citation xml:lang="en">Norris K, Vaughn C. The role of rennin-angiotensin-aldosterone system in chronic kidney disease. Expert Rev Cardiovasc Ther 2003; 1 (1): 51–63</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Nishiyama A, Yao L, Nagai Y, Miyata K, Yoshizumi M, Kagami S et al. Possible contributions of reactive oxygen species and mitogen-activated protein kinase to renal injury in aldosterone/salt-induced hypertensive rats. Hypertension2004; 43: 841–848</mixed-citation><mixed-citation xml:lang="en">Nishiyama A, Yao L, Nagai Y, Miyata K, Yoshizumi M, Kagami S et al. Possible contributions of reactive oxygen species and mitogen-activated protein kinase to renal injury in aldosterone/salt-induced hypertensive rats. Hypertension2004; 43: 841–848</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Blasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG. Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int 2003; 63: 1791–1800</mixed-citation><mixed-citation xml:lang="en">Blasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG. Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int 2003; 63: 1791–1800</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Peng H, Carretero OA, Raij L, Yang F, Kapke A, Rhaleb NE. Antifibrotic effects of N-acetyl-seryl-aspartyl-Lysyl-proline on the heart and kidney in aldosterone-salt hypertensive rats. Hypertension2001; 37: 794–800</mixed-citation><mixed-citation xml:lang="en">Peng H, Carretero OA, Raij L, Yang F, Kapke A, Rhaleb NE. Antifibrotic effects of N-acetyl-seryl-aspartyl-Lysyl-proline on the heart and kidney in aldosterone-salt hypertensive rats. Hypertension2001; 37: 794–800</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Nishiyama A, Abe Y. Molecular mechanisms and therapeutic strategies of chronic renal injury: renoprotective effects of aldosterone blockade. J Pharmacol Sci 2006; 1: 9–16</mixed-citation><mixed-citation xml:lang="en">Nishiyama A, Abe Y. Molecular mechanisms and therapeutic strategies of chronic renal injury: renoprotective effects of aldosterone blockade. J Pharmacol Sci 2006; 1: 9–16</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Greene EL, Kren S, Hostetter TH. Role of aldosterone in the remnant kidney model in the rat. J Clin Invest 1996; 98: 1063–1068</mixed-citation><mixed-citation xml:lang="en">Greene EL, Kren S, Hostetter TH. Role of aldosterone in the remnant kidney model in the rat. J Clin Invest 1996; 98: 1063–1068</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Rocha R, Chander PN, Khanna K, Zuckerman A, Stier CT Jr. Mineralocorticoid blockade reduces vascular injury in stroke-prone hypertensive rats. Hypertension 1998; 31: 451–458</mixed-citation><mixed-citation xml:lang="en">Rocha R, Chander PN, Khanna K, Zuckerman A, Stier CT Jr. Mineralocorticoid blockade reduces vascular injury in stroke-prone hypertensive rats. Hypertension 1998; 31: 451–458</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Brown NJ, Kim K-S, Chen Y-Q et al. Synergistic Effect of Adrenal Steroids and Angiotensin II on Plasminogen Activator Inhibitor-1 Production1. The Journal of Clinical Endocrinology &amp; Metabolism 2000; 85(1): 336–344</mixed-citation><mixed-citation xml:lang="en">Brown NJ, Kim K-S, Chen Y-Q et al. Synergistic Effect of Adrenal Steroids and Angiotensin II on Plasminogen Activator Inhibitor-1 Production1. The Journal of Clinical Endocrinology &amp; Metabolism 2000; 85(1): 336–344</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Connell JMC, Davies E. The new biology of aldosterone. Journal of Endocrinology 2005; 186: 1–20</mixed-citation><mixed-citation xml:lang="en">Connell JMC, Davies E. The new biology of aldosterone. Journal of Endocrinology 2005; 186: 1–20</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Cases A, Bragulat E, Serradell M et al. Endothelial dysfunction in chronic renal failure. Nephrologia 2003; 23(4): 42–51</mixed-citation><mixed-citation xml:lang="en">Cases A, Bragulat E, Serradell M et al. Endothelial dysfunction in chronic renal failure. Nephrologia 2003; 23(4): 42–51</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Landray MJ, Wheeler DС et al. Inflammation, Endothelial dysfunction and platelet activation in patients with chronic kidney disease: the chronic renal impairment in Birmingham (CRIB) Study. Am J Kidney Dis 2004; 43 (2): 244–253</mixed-citation><mixed-citation xml:lang="en">Landray MJ, Wheeler DС et al. Inflammation, Endothelial dysfunction and platelet activation in patients with chronic kidney disease: the chronic renal impairment in Birmingham (CRIB) Study. Am J Kidney Dis 2004; 43 (2): 244–253</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
